Biomedical subjects
Publications and source records attributed to R E Lewis.
The six species of Chaetopsylla Kohaut, 1903, two species of Polygenis Jordan, 1939, and one species of Rhopalopsyllus Baker, 1905 known to occur in North America north of Mexico are reviewed with respect to their host preferences and distribution. Keys are provided for the species, and their salient characters are illustrated.
The four genera and 11 species of bat fleas known to occur in North America north of Mexico are reviewed with respect to their distribution and host preferences. All are found on hosts belonging to the bat family Vespertilionidae except Sternopsylla distincta (Rothschild, 1903) and Hormopsylla trux Jordan, 1950, which parasitize species of Molossidae. Keys are provided for the genera and species and their diagnostic characters are illustrated.
The three species of Atyphloceras Jordan & Rothschild, 1915 and the four species of Hystrichopsylla Taschenberg, 1880 known to occur in North America north of Mexico are reviewed with respect to their host preferences and distribution. Keys are provided for the species, and their diagnostic characters are illustrated.
How the body successfully distinguishes its own tissue cells from those that are foreign and genetically nonidentical to it has been a focus of much research. Clonal deletion maintains that immune system cells with the potential to injure self constituents are eliminated during development, thereby neutralizing their capacity to induce self injury. Selected self-reactive maturing T cell clones undergo deletion in the thymus. A two-step selection process affects immature T cells that enter the thymus. Positive selection makes certain that all surviving cells are able to identify major histocompatibility complex (MHC) proteins present on all body cells. These MHC proteins interact with antigens and present them to T lymphocytes. Negative selection is essential for self-tolerance. It eliminates potentially injurious self-reactive T cells by placing them in contact with a mixture of self antigens in the thymus. Clonal anergy might act together with clonal deletion to maintain self tolerance. Self-reactive T cells in the blood of healthy subjects could represent cells whose affinities for antigen are too weak to initiate an immunologic disease. The fate of T cells reacting to a specific antigen has been traced in transgenic mice. Class I MHC molecules present peptides manufactured within the cell, whereas class II MHC molecules present peptides from extracellular proteins. Interaction of a T cell receptor with its homologous antigen associated with MHC molecules leads to proliferation of that T cell in the presence of costimulatory signals. Investigations elucidating the role of T cell receptors, MHC molecules and antigen peptides in self-nonself discrimination are discussed. The article concludes with an introductory summary of the remaining articles in the issue that address selected topics in self-nonself discrimination.
An inventory of all new taxa erected in the order Siphonaptera between 1 January 1984 and 31 December 1990 is presented. This includes one subfamily, five tribes, one genus, five subgenera, and 158 species and subspecies. Taxon accounts include the names of authors and publication sources, as well as collection data. Where known, the depository of the primary type is also included. An extensive bibliography is given as well as an updated supraspecific classification for the entire order based on studies published during the last decade.
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A complete inventory of the 307 currently valid genus-group names in the insect order Siphonaptera is given, along with their place of publication and type species.
The Tax protein from human T-cell leukemia virus type I (HTLV-I) is a 40-kDa phosphoprotein capable of activating transcription from its own long terminal repeat (LTR), as well as increasing the transcription of cellular genes. Transcriptional activation of the HTLV-I LTR has been demonstrated via a cyclic-AMP-responsive element within the 21-bp Tax-responsive elements of the LTR. Phorbol esters also upregulate expression via the LTR. Since phosphorylation of Tax may play a role in these processes, we investigated the relative effects of kinase-stimulating agents on 32P incorporation into Tax. Our studies demonstrated that the phorbol ester 4 beta-phorbol-12 beta-myristate-13 alpha-acetate greatly stimulated Tax phosphorylation in a time- and dose-dependent manner. In contrast, 8-bromoadenosine 3'-5'-cyclic monophosphate induced little stimulation of Tax phosphorylation. Tax phosphorylation occurred only on serine residues and was mapped to a single tryptic fragment in both Tax-producing human lymphocytes and mouse fibroblast cells.
Allopurinol is a potent xanthine oxidase inhibitor that has been administered to animals to protect tissues from oxidant injury. We hypothesized that allopurinol may protect against oxidant injury by inhibiting the inflammatory response. Male Sprague-Dawley rats were injected daily with vehicle or allopurinol and compared with noninjected controls. Animals were exposed to room air or 90% oxygen for 14 days. At the end of the exposure period, all animals were lavaged and bronchoalveolar lavage fluid (BALF) was examined for cell counts, lactate dehydrogenase (LDH), and protein. BALF neutrophils were significantly increased in oxygen-exposed noninjected controls (33 +/- 7 x 10(3)/mm3) and also in the vehicle-inoculated oxygen-exposed animals (43 +/- 6 x 10(3)/mm3). Allopurinol treatment resulted in a decrease in the neutrophilic alveolar response in oxygen-exposed animals (5.3 +/- 4 x 10(3)/mm3, P < 0.001). These data reveal that oxygen exposure produces a neutrophilic alveolar response that is attenuated by allopurinol treatment. BALF protein and LDH were significantly increased in all inoculated and noninoculated oxygen-exposed animals compared with air-exposed animals. Therefore, allopurinol decreases the neutrophilic alveolar response produced by a hyperoxic exposure in the rat but does not decrease lung injury as assessed by alveolar LDH and protein release.
Both natural and adaptive immune responses were found to be strikingly decreased 2 weeks after injury in 54 spinal cord injury and stroke patients, i.e., 28 quadriplegics, 21 paraplegics and 5 stroke patients, compared with those of age-matched controls. All values are expressed as means. Natural-killer (NK)-cell function decreased to 21.0% 2 weeks after spinal cord injury compared with 48.6% in controls. At 2 weeks, plasma ACTH values increased to 17.0 pg/ml in patients compared with 11.2 pg/ml in controls, and urine free cortisol levels were elevated to 162.4 micrograms/24 h in patients compared with 53.6 micrograms/24 h in controls. T-cell function decreased to 40.2% of normal (lymphocyte transformation) by 3 months after injury. T-cell activation (IL-2R) was diminished, i.e., 183.4 micrograms/ml compared with 328.2 micrograms/ml in controls. With rehabilitation therapy, NK-cell function increased to 41.6% by 7 months after injury. NK-cell-mediated lysis diminished sharply between 7 and 9 months, decreasing to 22.8% at 10 months and ultimately returning to the level seen 2 weeks after injury. Rehabilitation therapy contributed to the restoration of T-cell function to 92.0% of normal by 6 months after injury where it remained for 6+ months. IL-2R values improved in parallel with lymphocyte transformation. Whereas NK-cell-induced lysis remained depressed, i.e., 11.8% at 6 months and 11.4% at 12+ months in patients not receiving therapy, the restoration of NK-cell function at 6 months to 40.6% in rehabilitated patients decreased to 23.0% with cessation of treatment. NK-cell-mediated lysis values in cervical injury patients were significantly less than those in the thoracic injury group. Functional independence measurement (FIM) scores of the two paralleled their NK-cell function. With rehabilitation therapy, NK-cell-mediated lysis in the cervical group increased from 15.2 to 28.4%, whereas it improved in the thoracic group with therapy from 26.8 to 43.7%. With rehabilitation therapy, lymphocyte transformation in the cervical group increased from 37.3 to 85.6% and improved in the thoracic group from 48.4 to 88.9%. With rehabilitation therapy, FIM scores improved from 49.7 to 74.0 in the cervical group and from 79.8 to 97.3 in thoracic patients compared with 126 in controls. NK-cell-mediated lysis was depressed to 28.9% in 5 stroke patients and improved to 38.0% following rehabilitation therapy.
Transbronchial needle aspiration (TBNA) offers the unique opportunity to pathologically stage patients with lung cancer at the time of diagnostic bronchoscopy. The purpose of this study was to compare the staging sensitivities of the Wang 22-gauge and 19-gauge needles. We studied 64 patients with bronchogenic carcinoma and mediastinal adenopathy. Before bronchoscopy each patient underwent chest CT. Three to four aspirates were obtained with each needle from endotracheal sites adjacent to paratracheal lymphadenopathy. In 47 patients malignant mediastinal adenopathy was confirmed by the 19-gauge needle. A total of 29 patients had malignant 22-gauge needle aspirates. Of the 64 patients, 9 had benign, reactive mediastinal lymph nodes. There were 20 patients in whom only the 19-gauge needle demonstrated malignancy and 2 patients with malignant 22-gauge needle aspirates as the sole identifier of paratracheal malignancy. As a staging tool, the 19-gauge needle was significantly more sensitive than the 22-gauge needle, 85.5 versus 52.7% (p = 0.0001). Overall, in 49 of 55 patients (89.1%) with malignant mediastinal lymphadenopathy paratracheal tumor was confirmed by TBNA. The 19-gauge TBNA staging of the mediastinum is an effective, safe, and cost-saving alternative to surgical mediastinal exploration that can be performed during initial diagnostic bronchoscopy.
A semiquantitative heartworm test of antigen concentration was evaluated as a predictor of thromboembolism after adulticide treatment. Seventeen dogs with naturally acquired infections of Dirofilaria immitis (heartworms) were studied before and after thiacetarsamide treatment, using physical examinations, arterial blood gas analyses, thoracic radiography, and pulmonary hemodynamic and arteriographic tests. Eight dogs were considered to have a low burden of heartworms and 9 had a high burden. Dogs with a high worm burden had more severe pulmonary thromboembolism with pulmonary hypertension, dilated pulmonary arteries, flow obstruction of the caudal pulmonary arteries, and parenchymal lesions in the caudal lung lobes. Dogs with a low worm burden had minimal changes. Within each group of dogs, the severity of thromboembolism was less in some dogs in which all heartworms were not killed. Six of the 9 dogs with a high burden of heartworms had surviving heartworms, and 1 of these dogs had 38 live heartworms. Only 4 of the 8 dogs with a low worm burden had complete heartworm mortality, but only 1 dog had more than 3 surviving heartworms. We concluded that dogs with a high worm burden were more likely to have pulmonary thromboembolism after thiacetarsamide treatment and that dogs with a low worm burden were more likely to have minimal changes. A semiquantitative heartworm test of antigen concentration is recommended as part of the pretreatment evaluation of dogs infected with heartworms.
The severity of pulmonary thromboembolism and pulmonary hypertension induced by heartworms dying after administration of 2 adulticides was evaluated. Because melarsomine dihydrochloride (RM340) has been shown to be more effective in killing Dirofilaria immitis (heartworms) than the traditional approved adulticide, thiacetarsamide, an attempt was made to determine whether this new adulticide induced more severe lung disease. Before adulticide treatment, 32 dogs with naturally acquired heartworm infections received physical examinations, semiquantitative antigen concentration tests, CBC, platelet counts, serum biochemistry analyses, arterial blood gas determinations, thoracic radiography, pulmonary arteriography, and pulmonary hemodynamic tests. Eight dogs with a low burden and 9 dogs with a high burden of heartworms were treated with thiacetarsamide, and 7 dogs with a low burden and 8 dogs with a high burden were treated with RM340. Except for the heartworm-burden test, tests were repeated at regular intervals during the first 7 weeks after treatment. None of the dogs coughed or had dyspnea after treatment. Six of 9 dogs with high worm burdens and 4 of 8 dogs with low worm burdens had surviving heartworms after thiacetarsamide treatment, in contrast to only 3 of 15 RM340-treated dogs. Differences between the 2 adulticide treatments were minimal as determined by thoracic radiography, pulmonary hemodynamic tests, clinical laboratory analyses, pulmonary arteriography, or necropsy. The RM340 treatment was a more effective adulticide, but it did not increase the severity of hypertension and thromboembolism.
The protein kinase activity of human insulin receptors purified from Sf9 insect cells after infection with a recombinant baculovirus was evaluated. The following experimental observations led to the unexpected conclusion that this receptor protein catalyzes both serine and tyrosine autophosphorylation at significant stoichiometries. (i) Phosphorylation of lectin-purified insulin receptors with [gamma-32P]ATP resulted in rapid receptor tyrosine phosphorylation (7 mol of P per high-affinity binding site) and the delayed onset of insulin-stimulated receptor serine phosphorylation (about 7% of total phosphorylation). The tyrosine kinase inhibitor (hydroxy-2-naphthalenylmethyl)phosphonic acid (HNMPA), which has no effect on protein kinase C or cyclic AMP-dependent protein kinase activities, inhibited both the receptor serine and tyrosine phosphorylation. (ii) Phosphorylation of a synthetic peptide substrate composed of insulin receptor residues 1290-1319 on serines-1305/1306 by partially purified insulin receptors was also inhibited by HNMPA. (iii) Insulin receptors sequentially affinity-purified on immobilized wheat germ agglutinin and immobilized insulin showed no apparent contaminant proteins on silver-stained SDS/polyacrylamide gels yet catalyzed autophosphorylation on receptor serine and tyrosine residues when incubated with [gamma-32P]ATP. These results suggest that the catalytic site of the insulin receptor tyrosine kinase also recognizes receptor serine residues as substrates for the phosphotransfer reaction. Furthermore, insulin-stimulated receptor serine phosphorylation in intact cells may occur in part by an autophosphorylation mechanism subsequent to tyrosine phosphorylation of the insulin receptor.
Both natural and adaptive immune responses were shown to be strikingly decreased in initial blood samples from 34 spinal cord injury and stroke patients. NK-cell function decreased to 24.8% (mean) 2 weeks after spinal cord injury in previously healthy young adults whose control group revealed a mean NK-cell function of 48.7%. This was accompanied at 2 weeks by increased plasma ACTH (mean of 17.0 pg/ml from 17 patients compared to a mean of 11.2 pg/ml from 12 controls) and urine free cortisol levels (mean of 152.1 micrograms/24 h from 9 patients compared to 53.6 micrograms/24 h from 15 controls). T-cell function and/or activation decreased to below normal values within 3 months after injury as revealed by lymphocyte transformation that was 32.8% of normal at 3 months. T-cell activation diminished as shown by a mean IL-2 receptor level of 179.3 units/ml in patients compared to 328.2 units/ml in controls. Serial monitoring of NK- and T-cell function revealed that specific physical rehabilitation therapy over a period of 6 months after injury restored NK- and T-cell function to near normal levels in most patients. This improvement was accompanied by a parallel rise in the patient's functional independence measurement scores. Results suggest critical neuroendocrine-immune system interactions in the restoration of immune function. Cortisol levels reverted to normal after 6 months of rehabilitation. Limited data suggest that natural immune system depression, NK-cell function, persists in spinal cord injury patients not receiving rehabilitation therapy (mean NK-cell lysis of 10.3%; p < 0.01).
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In a previous investigation, we demonstrated an increased progression of overt AIDS in the African American population compared to the Caucasian population as reflected by the significantly lower absolute number of CD4+ lymphocytes detected in the African American population in an earlier study. The present study elucidates some of the possible genetic factors which may contribute to disease association or protection against HIV infection. The HLA phenotypes expressed as A, B, C, DR and DQw antigens were revealed by the Amos-modified typing procedure. NIH scoring was utilized to designate positive cells taking up trypan blue. A test of proportion equivalent to the chi 2 approximation was used to compare the disease population (n = 62; 38 African Americans, 24 Caucasians) to race-matched normal heterosexual local controls (323 African Americans, 412 Caucasians). Significant p values were corrected for the number of HLA antigens tested. HLA markers associated with possible protection from infection for African Americans were Cw4 and DRw6, whereas Caucasians expressed none. Disease association markers present in the African American population were A31, B35, Cw6, Cw7, DR5, DR6, DRw11, DRw12, DQw6 and DQw7, whereas in the Caucasian population A28, Aw66, Aw48, Bw65, Bw70, Cw7, DRw10, DRw12, DQw6 and DQw7 were demonstrated. The highest phenotypic frequency for a disease association marker in the study was for HLA-DR5 (62.9%) in the HIV-infected African American population without Kaposi's sarcoma compared to a frequency of 28.9% for the regional control group (p = 0.0012). We conclude that genetic factors do have a role in HIV infection since only 50-60% of those exposed to the AIDS virus will become infected.
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